No outside funding or services were received for this work. Outside of the current study, Bellows has received research funding from Biogen Idec, Regeneron Pharmaceuticals, Myriad Genetic Laboratories, Shire Development, and Bristol-Myers Squibb and an honorariam from Avanir Pharmaceuticals. Voelker received summer intern support from Pfizer and the AMCP Foundation during the time of this study. The remaining authors have nothing to disclose. All authors contributed to study concept and design and to the revision of the manuscript. Bellows, Olsen, and Voelker collected the data, assisted by Wander; data interpretation was performed primarily by Bellows, along with Olsen and Voelker and assisted by Wander. The manuscript was primarily written by Bellows, along with the other authors.
Aims To identify change in glycated haemoglobin (HbA1c) for 1 year after treatment intensification in patients with HbA1c >53 mmol/mol (7.0%) while on two classes of oral antidiabetic drugs (OADs). Material and methods A retrospective cohort study was conducted using a regional health plan claims database for the period January 1, 2010 to March 31, 2017. Patients with type 2 diabetes (T2DM) whose treatment was intensified with insulin, a glucagon‐like peptide‐1 receptor agonist or a third OAD within 365 days of having HbA1c ≥53 mmol/mol (7.0%) on two OADs were included. The HbA1c trajectory for 1 year after intensification was estimated using a mixed‐effects regression model. Results The analysis included 1226 patients with a mean ± SD HbA1c at treatment intensification of 74.2 ± 18.7 mmol/mol (8.93 ± 1.7%). HbA1c was higher in the insulin group (74.2 mmol/mol) than in the non‐insulin group (70.6 mmol/mol), as was the HbA1c decrease ( P < 0.01) over the 1‐year follow‐up, particularly in patients with baseline HbA1c >9%. After intensification, insulin‐ and non‐insulin‐treated patients achieved an average change by month in HbA1c of −4.7 mmol/mol and −2.6 mmol/mol points, respectively. The analysis predicted HbA1c to be the lowest at 6 to 10 months post intensification, depending on intensification treatment and HbA1c at intensification; however, on average, HbA1c remained above 64.0 mmol/mol (8.0%). Conclusion In patients with T2DM, intensification following an HbA1c value ≥53 mmol/mol (7.0%) while on two OADs was associated with a significant improvement in glycaemic control. Patients intensified with insulin had a higher baseline HbA1c but greater HbA1c reduction than those intensified with a non‐insulin agent. However, HbA1c remained above 64 mmol/mol (8.0%) overall. Additional opportunity exists to further intensify therapy to improve glycaemic control.
BACKGROUND: In the United States, more than 50% of patients with type 2 diabetes mellitus (T2DM) have hemoglobin A1c (A1c) levels that fail to achieve the recommended target of < 7.0%. Of these, 30%-45% have an A1c > 9.0%, the threshold for poorly controlled T2DM per National Committee for Quality Assurance (NCQA) measures. Treatment inertia is a known challenge. However, recent treatment intensification patterns and outcomes after treatment fails 2 classes of oral antidiabetic agents (OADs) are not well understood. OBJECTIVE: To characterize treatment intensification patterns and glycemic control outcomes in patients with A1c ≥ 7.0% on 2 OADs. METHODS: A retrospective cohort study was conducted in patients with T2DM from a regional health plan claims dataset augmented with A1c results between January 1, 2010, and March 31, 2017. Patients were identified with an A1c ≥ 7.0% (baseline), while on 2 OADs, and whose treatment was intensified with basal/biphasic insulin (insulin), glucagon-like peptide-1 receptor antagonist (GLP-1RA), or a third OAD within 365 days after the baseline A1c ≥ 7.0%. Patients had at least 1 A1c value 60-365 days (follow-up period) after treatment intensification. The proportion of patients with an A1c < 7.0% and < 9.0% at follow-up were identified by therapeutic intensification strategy. Odds ratios for achieving A1c < 7.0% and < 9.0% were calculated.RESULTS: 1,226 patients were included in the analysis, and 33.5% of the patients had a baseline A1c ≥ 9.0%. 24% of patients received insulin; 16% received GLP-1RA; and 60% received a third OAD for the treatment intensification. Overall, 26.0% achieved A1c < 7.0% and 76.1% of patients achieved < 9.0%, with a median follow-up of 119 days. The proportion of patients intensified with insulin who had an A1c ≥ 9.0% at follow-up was 34.6% versus 53.2% at baseline (P < 0.01). The corresponding percentages for those intensified with a GLP-1RA and OAD were 21.6% versus 27.1% (P = 0.24) and 20.1% versus 27.3% (P < 0.01). After controlling for baseline characteristics, the odds ratio (95% CI) of achieving A1c < 7.0% and < 9.0% was 2.05 (1.45-2.90) for GLP-1RA and 0.92 (0.61-1.40) for OAD. The association between goal attainment and GLP-1RA versus OAD intensification was influenced by the time to the A1c follow-up and baseline A1c.CONCLUSIONS: Treatment intensification was associated with improved glycemic control in patients after therapy failed 2 OADs. Patients with higher A1c at baseline were likely to initiate insulin, which was associated with a greater drop in A1c. GLP-1RA was associated with a higher likelihood of achieving NCQA-suggested glycemic control compared with a third OAD. However, the association varied by the follow-up period. These findings are important to health plans seeking to improve patient outcomes as reflected in high performance on NCQA diabetes quality measures by promoting effective and timely treatment intensification.
This study was funded by Regeneron Pharmaceuticals and Sanofi US. Boklage is employed by, and owns stock in, Regeneron, and Charland is employed by Sanofi. Bellows has received fees from Avenir for advisory board membership and grants from Myriad Genetics, Biogen, Janssen, and National Institutes of Health. Brixner reports advisory board and consultancy fees and grants from Sanofi. Mitchell reports consultancy fees from Sanofi. Study concept and design were contributed by Bellows, Boklage, Charland, and Brixner. Bellows, Sainski-Nguyen, and Olsen took the lead in data collection, along with Mitchell. Data interpretation was performed by Mitchell, along with the other authors. The manuscript was written by Bellows, Sainski-Nguyen, and Olsen and revised by all the authors.
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